Korean American Female Educators\u27 Self Concept and Perception Toward School Leadership

Asian American educators and school leaders’ leading the K-12 educational system have been under researched and under-theorized. Asian American populations is one of the fastest growing populations in the United States, and Asian American educators’ experiences and contributions cannot be ignored in educational policy, teacher education and research. The following study is to contribute to the body of existing research to the voices of Asian American female educators and school leaders through the study of Korean American female educators of long term and short term residents in the U.S.- their self-concept and their experiences that limits or enables them to become school leaders. Drawing from Sociocultural theory, an Asian Critical Theory, and Super’s Theory of Career Stages, the following comparative non-experimental study first employed semi-structured, open-ended interviews of six long and short term U.S. resident school leaders and teachers who have identified themselves as Korean American female educators. Transcribed interviews were coded for themes and used their expressions and vocabulary to construct appropriate questions and survey items for data collection that enabled or limited Korean American female educators to become educational leaders. The survey items were sent to 200-300 Korean American female educators via emails through Google Form. Results showed that there was a significant difference in the perception toward leadership, experience of stereotype and influence of ethnic/familial culture and cultural role as females on the number of years of employment, years of residence in the US (long term vs. short term) and on the employment status as a teacher or as a school leader. This study will add to the recruitment and diversification of American educational leadership, how they experience the profession and the lack of Korean American female educational leaders at this time

Kes perniagaan Sabah : kajian intensification of research in priority areas (lRPA)

No. abstrac

Socioeconomic disparities in behavioral risk factors and health outcomes by gender in the Republic of Korea

<p>Abstract</p> <p>Background</p> <p>Few studies have examined socioeconomic disparities in health and behavioral risk factors by gender in Asian countries and in South Korea, specifically. We investigated the relationship between socioeconomic position (education, income, and occupation) and subjective and acute and chronic health outcomes and behavioral risk factors by gender, and compared results from 1998 and 2005, in the Republic of Korea.</p> <p>Methods</p> <p>We examined data from a nationally representative stratified random sample of 4213 men and 4618 women from the 1998 Korea National Health and Nutrition Examination Survey, and 8289 men and 8827 women from the 2005 Korea National Health and Nutrition Examination Survey using General Linear Modeling and multiple logistic regression methods.</p> <p>Results</p> <p>Controlling for behavioral risk factors (smoking, drinking, obesity, exercise, and sleep), those in lower socioeconomic positions had poorer health outcomes in both self-reported acute and chronic disease and subjective measures; differences were especially pronounced among women. A socioeconomic gradient for education and income was found for both men and women for morbidity and self-reported health status, but the gradient was more pronounced in women. In 1998, the odds ratios (ORs) of higher morbidity for illiterate vs. college educated females was 5.4:1 and 1.9:1 for females in the lowest income quintile vs. the highest. The OR for education decreased in 2005 to 2.9:1 and that for income quintiles remained the same at 1.9:1. The OR of lower self-reported health status for illiterate vs. college educated females was 2.9:1 and 1.6:1 for females in the lowest income quintile vs. the highest in 1998, and 3.3:1 and 2.3:1 in 2005.</p> <p>Conclusions</p> <p>Among Korean adults, men and women in lower socioeconomic position, as denoted by education, income, and somewhat less by occupation, experience significantly higher levels of morbidity and lower self-reported health status, even after controlling for standard behavioral risk factors. Disparities were more pronounced for women than for men. Efforts to reduce health disparities in South Korea require attention to the root causes of socioeconomic inequality and gender differences in the impact of socioeconomic position on health.</p

Skewed Distribution of Circulating Activated Natural Killer T (NKT) Cells in Patients with Common Variable Immunodeficiency Disorders (CVID)

Common variable immunodeficiency disorder (CVID) is the commonest cause of primary antibody failure in adults and children, and characterized clinically by recurrent bacterial infections and autoimmune manifestations. Several innate immune defects have been described in CVID, but no study has yet investigated the frequency, phenotype or function of the key regulatory cell population, natural killer T (NKT) cells. We measured the frequencies and subsets of NKT cells in patients with CVID and compared these to healthy controls. Our results show a skewing of NKT cell subsets, with CD4+ NKT cells at higher frequencies, and CD8+ NKT cells at lower frequencies. However, these cells were highly activated and expression CD161. The NKT cells had a higher expression of CCR5 and concomitantly expression of CCR5+CD69+CXCR6 suggesting a compensation of the remaining population of NKT cells for rapid effector action

NIK Stabilization in Osteoclasts Results in Osteoporosis and Enhanced Inflammatory Osteolysis

Maintenance of healthy bone requires the balanced activities of osteoclasts (OCs), which resorb bone, and osteoblasts, which build bone. Disproportionate action of OCs is responsible for the bone loss associated with postmenopausal osteoporosis and rheumatoid arthritis. NF-κB inducing kinase (NIK) controls activation of the alternative NF-κB pathway, a critical pathway for OC differentiation. Under basal conditions, TRAF3-mediated NIK degradation prevents downstream signaling, and disruption of the NIK:TRAF3 interaction stabilizes NIK leading to constitutive activation of the alternative NF-κB pathway.Using transgenic mice with OC-lineage expression of NIK lacking its TRAF3 binding domain (NT3), we now find that alternative NF-κB activation enhances not only OC differentiation but also OC function. Activating NT3 with either lysozyme M Cre or cathepsinK Cre causes high turnover osteoporosis with increased activity of OCs and osteoblasts. In vitro, NT3-expressing precursors form OCs more quickly and at lower doses of RANKL. When cultured on bone, they exhibit larger actin rings and increased resorptive activity. OC-specific NT3 transgenic mice also have an exaggerated osteolytic response to the serum transfer model of arthritis.Constitutive activation of NIK drives enhanced osteoclastogenesis and bone resorption, both in basal conditions and in response to inflammatory stimuli

Comparative evaluation of the treatment efficacy of suberoylanilide hydroxamic acid (SAHA) and paclitaxel in ovarian cancer cell lines and primary ovarian cancer cells from patients

BACKGROUND: In most patients with ovarian cancer, diagnosis occurs after the tumour has disseminated beyond the ovaries. In these cases, post-surgical taxane/platinum combination chemotherapy is the "gold standard". However, most of the patients experience disease relapse and eventually die due to the emergence of chemotherapy resistance. Histone deacetylase inhibitors are novel anticancer agents that hold promise to improve patient outcome. METHODS: We compared a prototypic histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), and paclitaxel for their treatment efficacy in ovarian cancer cell lines and in primary patient-derived ovarian cancer cells. The primary cancer cells were isolated from malignant ascites collected from five patients with stage III ovarian carcinomas. Cytotoxic activities were evaluated by Alamar Blue assay and by caspase-3 activation. The ability of SAHA to kill drug-resistant 2780AD cells was also assessed. RESULTS: By employing the cell lines OVCAR-3, SK-OV-3, and A2780, we established SAHA at concentrations of 1 to 20 μM to be as efficient in inducing cell death as paclitaxel at concentrations of 3 to 300 nM. Consequently, we treated the patient-derived cancer cells with these doses of the drugs. All five isolates were sensitive to SAHA, with cell killing ranging from 21% to 63% after a 72-h exposure to 20 μM SAHA, while four of them were resistant to paclitaxel (i.e., <10% cell death at 300 nM paclitaxel for 72 hours). Likewise, treatment with SAHA led to an increase in caspase-3 activity in all five isolates, whereas treatment with paclitaxel had no effect on caspase-3 activity in three of them. 2780AD cells were responsive to SAHA but resistant to paclitaxel. CONCLUSION: These ex vivo findings raise the possibility that SAHA may prove effective in the treatment of paclitaxel-resistant ovarian cancer in vivo

The Onconeural Antigen cdr2 Is a Novel APC/C Target that Acts in Mitosis to Regulate C-Myc Target Genes in Mammalian Tumor Cells

Cdr2 is a tumor antigen expressed in a high percentage of breast and ovarian tumors and is the target of a naturally occurring tumor immune response in patients with paraneoplastic cerebellar degeneration, but little is known of its regulation or function in cancer cells. Here we find that cdr2 is cell cycle regulated in tumor cells with protein levels peaking in mitosis. As cells exit mitosis, cdr2 is ubiquitinated by the anaphase promoting complex/cyclosome (APC/C) and rapidly degraded by the proteasome. Previously we showed that cdr2 binds to the oncogene c-myc, and here we extend this observation to show that cdr2 and c-myc interact to synergistically regulate c-myc-dependent transcription during passage through mitosis. Loss of cdr2 leads to functional consequences for dividing cells, as they show aberrant mitotic spindle formation and impaired proliferation. Conversely, cdr2 overexpression is able to drive cell proliferation in tumors. Together, these data indicate that the onconeural antigen cdr2 acts during mitosis in cycling cells, at least in part through interactions with c-myc, to regulate a cascade of actions that may present new targeting opportunities in gynecologic cancer

Expression of Stretch-Activated Two-Pore Potassium Channels in Human Myometrium in Pregnancy and Labor

Background: We tested the hypothesis that the stretch-activated, four-transmembrane domain, two pore potassium channels (K2P), TREK-1 and TRAAK are gestationally-regulated in human myometrium and contribute to uterine relaxation during pregnancy until labor. Methodology: We determined the gene and protein expression of K2P channels in non-pregnant, pregnant term and preterm laboring myometrium. We employed both molecular biological and functional studies of K2P channels in myometrial samples taken from women undergoing cesarean delivery of a fetus. Principal Findings: TREK-1, but not TREK-2, channels are expressed in human myometrium and significantly up-regulated during pregnancy. Down-regulation of TREK-1 message was seen by Q-PCR in laboring tissues consistent with a role for TREK-1 in maintaining uterine quiescence prior to labor. The TRAAK channel was unregulated in the same women. Blockade of stretch-activated channels with a channel non-specific tarantula toxin (GsMTx-4) or the more specific TREK-1 antagonist L-methionine ethyl ester altered contractile frequency in a dose-dependent manner in pregnant myometrium. Arachidonic acid treatment lowered contractile tension an effect blocked by fluphenazine. Functional studies are consistent with a role for TREK-1 in uterine quiescence. Conclusions: We provide evidence supporting a role for TREK-1 in contributing to uterine quiescence during gestation an

Mitochondrial Structure, Function and Dynamics Are Temporally Controlled by c-Myc

Although the c-Myc (Myc) oncoprotein controls mitochondrial biogenesis and multiple enzymes involved in oxidative phosphorylation (OXPHOS), the coordination of these events and the mechanistic underpinnings of their regulation remain largely unexplored. We show here that re-expression of Myc in myc−/− fibroblasts is accompanied by a gradual accumulation of mitochondrial biomass and by increases in membrane polarization and mitochondrial fusion. A correction of OXPHOS deficiency is also seen, although structural abnormalities in electron transport chain complexes (ETC) are not entirely normalized. Conversely, the down-regulation of Myc leads to a gradual decrease in mitochondrial mass and a more rapid loss of fusion and membrane potential. Increases in the levels of proteins specifically involved in mitochondrial fission and fusion support the idea that Myc affects mitochondrial mass by influencing both of these processes, albeit favoring the latter. The ETC defects that persist following Myc restoration may represent metabolic adaptations, as mitochondrial function is re-directed away from producing ATP to providing a source of metabolic precursors demanded by the transformed cell